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Microbiome in Atopic Dermatitis: Is It All About Staphylococcus aureus?

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Abstract

Purpose of Review

There are many recent informative reviews about the skin microbiome in atopic dermatitis (AD) highlighting the prominent role of Staphylococcus aureus (S. aureus) in the pathogenesis of this skin disease. The aim of the current review is to compile and discuss the findings of original studies describing other microbiota alterations contributing to atopic skin inflammation. Moreover, we will discuss the feasibility of using these identified alterations as future diagnostic or therapeutic strategies.

Recent Findings

Besides S. aureus, there is evidence that other species could also be deleterious in AD, such as the commensal S. epidermidis. Furthermore, microbial metabolites produced by commensal are lost during microbiota dysbiosis; thereby further contributing to AD pathogenesis. Among those, metabolites interacting with the aryl hydrocarbon receptor (AhR), such as metabolites of the tryptophan (Trp) pathway or short chain fatty acids (SCFA) are of special interest since they are able to modulate the transcription of epithelial alarmin genes. Although S. aureus plays a major role in AD pathogenesis, other species and, perhaps more importantly, the metabolites or enzymes they produce may modulate AD pathogenesis.

Summary

These findings offer future avenues to explore diagnostic or therapeutic approaches for atopic skin inflammation.

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CGC, ZU and PO declare that they have no conflict of interest. BH reports grants and personal fees from Galderma, personal fees from Pfizer, personal fees from Eli Lilly, personal fees from Novartis, personal fees from Boehringer Ingelheim, personal fees from Janssen, personal fees from Sanofi, personal fees from LEO Pharma, personal fees from AbbVie, and personal fees from Celgene, outside the submitted work.

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Gomez-Casado, C., Unger, Z., Olah, P. et al. Microbiome in Atopic Dermatitis: Is It All About Staphylococcus aureus?. Curr Treat Options Allergy 10, 351–363 (2023). https://doi.org/10.1007/s40521-023-00350-9

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